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CMV Serology:
This test is not recommended for baseline screening in the 2008 NIH/CDC/IDSA Guidelines for Prevention and Treatment of Opportunistic Infections (http://aidsinfo.nih.gov) due to limited clinical utility in most patients although a negative test usually excludes CMV disease (Ann Intern Med 1993;118:12; Lancet 2004; Lancet 2004;363:2116). Possible uses of serology: 1) identification of seronegative patients for counseling on CMV prevention (although the message is not different from the "safe sex message" for preventing HIV transmission); 2) assessment of the likelihood of CMV disease in late-stage HIV infection; 3) identification of seronegative individuals who should receive CMV-antibody-negative blood or leukocyte-reduced blood products for nonemergent trans-fusions (JAMA 2001;285:1592). Sero - prevalence for adults in the United States is about 50%; in MSM and injection drug users it is >90% (JID 1985;152:243; Am J Med 1987;82:593). It should be noted there are multiple methods to detect CMV, including p65 antigen assays, CMV DNA PCR assays, NASBA early antigen assays, and culture of blood and urinary tests using culture and urinary CMV DNA PCR. None of the tests has proven effective in predicting CMV disease in HIV-infected persons (J Clin Microbiol 2000;38:563).
Glucose-6-Phosphate Dehydrogenase Levels (G6-PD): G6-PD deficiency is a genetic disease that predisposes to hemolytic anemia following exposure to oxidant drugs commonly such as dapsone, primaquine and TMP-SMX. Over 150 G6-PD variants are inherited on the X chromosome, but the most frequent are GdA-, which is found in 10% of black men and in 1% to 2% of black women, and Gdmed, found predominantly in men from the Mediterranean area ( Italians, Greeks, Sephardic Jews, Arabs), India, and Southeast Asia. With most defects, the hemolysis is mild and self-limited because only the older red cells are involved, and the bone marrow can compensate even with continued administration of the implicated drug. The important exception is Gdmed, which may cause life-threatening hemolysis. The limited hemolysis in patients with GdA- may be significant in patients with HIV infection, who often have anemia from other causes. The severity of anemia also depends on the concentration of the drug in red cells and the oxidant potential of the inducing agent. The most likely offending agents are dapsone and primaquine. Sulfonamides cause hemolysis less commonly. G6-PD deficiency may be partial, in which case the contraindication for oxidant drugs is relative. Options for screening include: 1) test at baseline in all patients; 2) restrict testing to those most likely to have a defect or when oxidant drugs are anticipated; and 3) reserve testing for the occasional case of hemolytic anemia following exposure to typical inducing agents. Typical findings with this hemolysis include elevated indirect bilirubin, elevated LDH, decreased haptoglobin, methemoglobinemia, reticulocytosis, and aperipheral
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